Pulido et al. [ 80 ] has published the only study to date investigating the effect of Cr supplementation on intracellular Ca 2+ handling in dystrophic muscle. Cultured mdx myotubes were supplemented in vitro with 30 mM Cr at the onset of myocyte fusion and cytoplasmic Ca 2+ was quantified using the Ca 2+ -specific fluorophore Fura-2. Cr was shown to significantly inhibit dystrophy-induced sarcoplasmic elevations in Ca 2+ concentration after several days of supplementation. This was attributed to enhanced SR Ca 2+ ATPase activity, albeit direct measurement of SR Ca 2+ was not made and thus improvements in sarcolemmal and mitochondrial ATPase activity could not be ruled out. Ca 2+ influx rates remained unaffected between Cr-supplemented and unsupplemented groups, indicating definite improvements in Ca 2+ buffering capacity rather than a reduction in entry [ 80 ]. This study most importantly demonstrated that Cr-induced improvements in sarcoplasmic Ca 2+ buffering and improved myotube survival rates [ 80 ]. An extension of this research by Passaquin et al. [ 83 ] supported Pulido’s findings, demonstrating delayed onset and reduced severity of initial degenerative cycles in young mice, which was accompanied by enhanced mitochondrial oxidative function. Whilst the findings of Pulido et al. [ 80 ] and Passaquin et al. [ 83 ] differ from those of Louis et al. [ 81 ] with respect to the effects of Cr supplementation on skeletal muscle Ca 2+ handling, it is possible that the absolute gastrocnemius Ca 2+ concentration ascertained by Louis et al. [ 81 ] is misrepresentative of the fact that Cr supplementation might increase cell survival duration by increasing the buffering of Ca 2+ from the sarcoplasm into subcellular compartments and retaining it within. Thus whilst a greater net Ca 2+ concentration of myofibres would be observed, relative sarcoplasmic Ca 2+ concentration would be significantly decreased by the better Ca 2+ buffering capacity afforded by Cr. That CK is demonstrably linked to the sarco(endo)plasmic reticulum Ca 2+ ATPase (SERCA) indeed indicates that improved uptake into the SR is likely [ 84 , 85 ], and thus that maintaining energy homeostasis in fundamental to moderating the pathological damage of dystrophin-deficient skeletal muscle.